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Related Concept Videos

Parkinson Disease ll: Pathophysiology01:24

Parkinson Disease ll: Pathophysiology

Parkinson disease (PD) is a progressive neurodegenerative disorder primarily affecting movement, with additional non-motor features. Its pathophysiology involves complex interactions among genetic susceptibility, environmental exposures, and cellular dysfunction, including dopaminergic neuron loss, protein aggregation, and mitochondrial impairment.Selective NeurodegenerationA key feature is the degeneration of dopaminergic neurons in the substantia nigra pars compacta, leading to reduced...
Neural Regulation01:37

Neural Regulation

Digestion begins with a cephalic phase that prepares the digestive system to receive food. When our brain processes visual or olfactory information about food, it triggers impulses in the cranial nerves innervating the salivary glands and stomach to prepare for food.
Parkinson's Disease: Overview01:15

Parkinson's Disease: Overview

Neurodegenerative disorders are progressive diseases that cause irreversible damage and loss to neurons in specific brain areas. Examples of these disorders include Parkinson's disease, Alzheimer's disease, Multiple Sclerosis (MS), and Amyotrophic Lateral Sclerosis (ALS). These disorders share characteristics such as proteinopathies, selective neuronal vulnerability, and a complex interplay between genetic and environmental factors. The primary therapeutic goal for these conditions is to...
Parkinson Disease l: Introduction01:24

Parkinson Disease l: Introduction

Parkinson’s disease is a chronic, progressive neurodegenerative disorder that primarily affects movement. It is characterized by motor symptoms such as resting tremors, muscle rigidity, bradykinesia (slowness of movement), and postural instability. Patients may notice hand tremors at rest, stiffness during movement, or a shuffling gait. In addition to motor features, non-motor symptoms include sleep disturbances, mood and behavioral changes, constipation, and cognitive impairment, all of which...
Amyloid Fibrils03:03

Amyloid Fibrils

Amyloid fibrils are aggregates of misfolded proteins.  Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils. 
Amyloid deposits were observed as early as 1639 in the liver and the spleen.   In 1854, Rudolph Virchow performed iodine staining, normally used to...
Lysosomal Hydrolases01:22

Lysosomal Hydrolases

Lysosomes are the site for the degradation of macromolecules and biological polymers released during membrane trafficking events such as secretory, endocytic, autophagic, and phagocytic pathways. The membrane-enclosed area of the lysosome, called the lumen, contains hydrolytic enzymes active in an acidic environment. These acid hydrolases are functional at a pH between 4.5 and 5 and are involved in cellular processes such as cell signaling, energy metabolism, restoration of the plasma membrane,...

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Related Experiment Video

Updated: Jun 5, 2026

Detection of Disease-associated α-synuclein by Enhanced ELISA in the Brain of Transgenic Mice Overexpressing Human A53T Mutated α-synuclein
12:01

Detection of Disease-associated α-synuclein by Enhanced ELISA in the Brain of Transgenic Mice Overexpressing Human A53T Mutated α-synuclein

Published on: May 30, 2015

CSF α-synuclein does not differentiate between parkinsonian disorders.

M B Aerts1, R A J Esselink, W F Abdo

  • 1Department of Neurology, Parkinson Center Nijmegen (ParC), Donders Institute for Brain, Cognition and Behaviour, Radboud University Nijmegen Medical Centre, the Netherlands.

Neurobiology of Aging
|January 18, 2011
PubMed
Summary

Cerebrospinal fluid (CSF) alpha-synuclein levels do not reliably distinguish Parkinson's disease (PD) from atypical Parkinsonism (AP). This study found no significant differences, suggesting CSF alpha-synuclein is not a suitable biomarker for differentiating these conditions.

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Detection of Disease-associated α-synuclein by Enhanced ELISA in the Brain of Transgenic Mice Overexpressing Human A53T Mutated α-synuclein
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Targeting Alpha Synuclein Aggregates in Cutaneous Peripheral Nerve Fibers by Free-floating Immunofluorescence Assay

Published on: June 25, 2019

Area of Science:

  • Neurology
  • Biochemistry
  • Biomarker Discovery

Background:

  • Distinguishing Parkinson's disease (PD) from atypical Parkinsonism (AP) is crucial for effective treatment and patient management.
  • Accurate diagnosis aids in targeted therapies, patient counseling, and early identification of disease-specific complications.

Purpose of the Study:

  • To evaluate the diagnostic utility of cerebrospinal fluid (CSF) alpha-synuclein concentrations in differentiating PD from AP.
  • To determine if CSF alpha-synuclein can serve as an additional biomarker for differential diagnosis in parkinsonism.

Main Methods:

  • Analyzed CSF samples from 142 parkinsonism patients (including PD, MSA, DLB, VaP, PSP, CBD) using clinical diagnosis after 2-year follow-up as the gold standard.
  • Measured CSF concentrations of alpha-synuclein, blood pigments, and erythrocyte count.
  • Statistical analysis adjusted for age, disease severity, and presence of blood contaminants.

Main Results:

  • No significant differences were observed in CSF alpha-synuclein concentrations between patients with PD and healthy controls.
  • No significant differences were found when comparing PD patients to the overall atypical Parkinsonism (AP) group or its subgroups.
  • Adjustments for potential confounding factors did not alter these findings.

Conclusions:

  • CSF alpha-synuclein is currently unsuitable as a standalone biomarker for differentiating Parkinson's disease from atypical Parkinsonism.
  • Further research may be needed to explore other biomarkers or combinations for improved diagnostic accuracy in parkinsonism.